Speaker 1: Today we're gonna be going over gastric disorders, so it's
Speaker 1: going to be involving gastritis, peptic ulcer disease, and pyloric stenosis.
Speaker 1: And I just want to mention really quick, if you
Speaker 1: do like the podcast, it's helping you. Please, please, if
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Speaker 1: just let me know that it's helping you. It kind
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Speaker 1: So with that being said, let's go ahead and start
Speaker 1: with aqte gastritis. So qute gastritis is an inflammation resulting
Speaker 1: from gastric mucosal injury. It's important to note that there
Speaker 1: is something else called gastropathy, which is going to be
Speaker 1: a more superficial mucosal injury with no associated inflammation. So
Speaker 1: that's another term that you need to know as well.
Speaker 1: As far as eteologies, H pylori most common cause by
Speaker 1: far H pylori. Remember this is going to be your
Speaker 1: most common cause of acte gastritis.
Speaker 2: And H.
Speaker 1: Pylori is a GRAM negative bacteria that's very common. It's
Speaker 1: actually found in about half of the world's population, So
Speaker 1: not everybody gets symptoms from this though, So just because
Speaker 1: it's part of your microbio doesn't mean you're gonna have symptoms,
Speaker 1: but the people that do develop symptoms. H Pylori infects
Speaker 1: the gastric mucosa. It releases certain enzymes and toxins, and
Speaker 1: it injures the epithelial cells of the stomach, which leaves
Speaker 1: the stomach more vulnerable to the acid that's present and
Speaker 1: causes gastritis. It can cause peptic ulcers as well as
Speaker 1: pain and a number of other symptoms. So that's how
Speaker 1: H bilori causes that. Again, most common cause. That keep
Speaker 1: repeating it because it's important. And then your second most
Speaker 1: common cause is going to be from n seds and aspirin.
Speaker 1: So the way n seds and aspirin and cause gastritis
Speaker 1: one way is that it's just from a superficial irritation
Speaker 1: of the epithelium of the gastric mucosa. So that can
Speaker 1: happen if you take like eight hundred milligrams vibuprof and
Speaker 1: you didn't any food with it, and you just have
Speaker 1: this stomach pain for a couple hours. But the more
Speaker 1: important factor is that n sets inhibit COX one production,
Speaker 1: so COX one production is actually responsible for producing prostag landins.
Speaker 1: So if you decrease COX one production, decrease production of
Speaker 1: prostic landings. Well, why does that matter. It's because prostac
Speaker 1: landins actually inhibit gastric acid secretion, so less prostac landins
Speaker 1: means more gastric acid and more irritation like gastritis peptic ulcers.
Speaker 1: So that's why n sets are really important as a
Speaker 1: factor that can cause gastritis. And that's actually why n
Speaker 1: sets like celebres, which is also known as celocoxid, were
Speaker 1: created because celebres actually targets COX two rather than COX one,
Speaker 1: So this leads to less gastric issues and they have
Speaker 1: a number of other cardiovascular problems, but that's besides the point.
Speaker 1: But that's why they were created because when you don't
Speaker 1: target COX one, you don't affect the prostac landids in
Speaker 1: the stomach and you have less gastric problems. So that's
Speaker 1: why nc's are a big issue here. Some other less
Speaker 1: important causes are going to be alcohol, trauma, acute stress,
Speaker 1: radiation and things like that, but the ones you need
Speaker 1: to know is going to be h pylori and n sets.
Speaker 1: Do not forget those H pyloris You're most common and
Speaker 1: says you're second most common costs.
Speaker 2: So remember those.
Speaker 1: As far as the patient presentation, some patients initially may
Speaker 1: be asymptomatic, but as it progresses, you're going to have
Speaker 1: these non specific symptoms. It's like epigastric discomfort also known
Speaker 1: as dyspepsia. They may have some nausea, loss of appetite,
Speaker 1: nothing really specific that you need to know that's gonna
Speaker 1: stick out in a vignette, but just these non specific
Speaker 1: epigastric symptoms. Diagnosing while your test of choice, although it
Speaker 1: isn't necessarily going to be the first thing you do,
Speaker 1: is going to be an upper endoscopy. This is going
Speaker 1: to be your best test. But initially you're going to
Speaker 1: do some testing for H pylori because these are things
Speaker 1: that are non invasive. You can do a uria breath test,
Speaker 1: a fecal antigen test to test for H pylori to
Speaker 1: see if you need to treat that. I'll go over
Speaker 1: those tests a little bit in pepticals or disease and
Speaker 1: what they involve, but those so initially you probably test
Speaker 1: for h uria breath test fecal antigen test, and then eventually,
Speaker 1: if those tests come back negative, these patients are still
Speaker 1: having symptoms, you may move on to an upper endoscopy,
Speaker 1: which would be your best test. And this is going
Speaker 1: to be patients that are refractory to PPIs, H two
Speaker 1: blockers things like that. So some of the ways you
Speaker 1: can diagnose test for H pylori, upper endoscopy, and treatment, well,
Speaker 1: it all depends on the cause. So if these patients
Speaker 1: have H pylori, your test came back positive, you're your
Speaker 1: breath test or vecal antigen test came back positive. You're
Speaker 1: going to treat H pylori. So how do you treat
Speaker 1: H pyloria, whether it's quadruple therapy. Quadruple therapy is going
Speaker 1: to be a combination of PPIs, bismuth, metronidazol, and tetracycling.
Speaker 1: So H pylori positive treat the H pylori with quadruple therapy.
Speaker 1: You want to discontinue n SAID use if that's what's
Speaker 1: causing it, and you can also use PPIs and H
Speaker 1: two blockers, particularly in patients who require the continued use
Speaker 1: of n SET. So whether it's a cardiovascular patient that
Speaker 1: requires daily aspirin patient with chronic pain that has to
Speaker 1: take their ND sets but they develop gastritis, then you
Speaker 1: can use PPIs and H two blockers as well for
Speaker 1: the treatment. So treatment depends on the cause H pylori.
Speaker 1: Treat the H pylori discontinue n said use if they're
Speaker 1: using it, and PPIs and H two blockers are going
Speaker 1: to be your main.
Speaker 2: Ways to treat qute gastritis.
Speaker 1: As something else that I'm going to go over, it's
Speaker 1: definitely not very high yield, but you need to know
Speaker 1: that it exists because it is on the blueprint. It's
Speaker 1: something called autoimmune metaplastic atrophic gastritis, so again not high yield,
Speaker 1: but be aware that it exists. It's a chronic form
Speaker 1: of gastritis. It's an inherited autoimmune disease, so unlike a
Speaker 1: cute gastritis, this isn't going to be from N sets
Speaker 1: or it's pylori use. It's going to be an autoimmune process.
Speaker 1: So the immune system is actually attacking the parietal cells,
Speaker 1: an intrinsic factor in the body. This can lead to
Speaker 1: B twelve deficiency as well as this gastritis that these
Speaker 1: patients have. These patients are also at a high risk
Speaker 1: of gastric carcinoma.
Speaker 2: And one other important thing.
Speaker 1: That you need to know is that while acute gastritis
Speaker 1: most commonly affects the antrum of the stomach, chronic or
Speaker 1: autoimmune gastritis spares the antrum and most commonly affects the
Speaker 1: fundus or the body. So for real life maybe not
Speaker 1: so important, but for a vin yet they may mention that.
Speaker 1: So remember a QT gastritis affects the antrum, chronic autoimmune
Speaker 1: is going to most commonly affect the fundus in the
Speaker 1: body and spares the andantrum. That's really all you need
Speaker 1: to know for that. Don't go crazy again, not very
Speaker 1: high yield.
Speaker 2: Now moving on.
Speaker 1: To something that is high yield is peptic ulcer disease.
Speaker 1: So there's a lot of stuff you need to know
Speaker 1: on this. Let's go over that. There's going to be
Speaker 1: some overlap two with gastritis as well. So peptic ulcer
Speaker 1: disease encompasses both duodenal ulcers and gastric ulcers. So some
Speaker 1: things that two have in common, some things that help
Speaker 1: differentiate them. So we'll go over the different things. So
Speaker 1: let's start with duoden ulcers so duoden ulcers are going
Speaker 1: to be an area of erosion obviously in the duodenum.
Speaker 1: It's going to be your most common type, so much
Speaker 1: more common, about four times more common than gastric ulcers,
Speaker 1: and usually it's benign. Gastric Ulcers are going to be
Speaker 1: an area of erosion in the stomach, and these are
Speaker 1: less prevalent than duodenal ulcers and more commonly associated with
Speaker 1: gastric edinal carcinoma. So remember that duodenal ulcers usually benign.
Speaker 1: Gastric ulcers are more commonly associated with gastric adino carcinoma,
Speaker 1: and duoden ulcers are your more common type as far
Speaker 1: as eteologies, a lot of overlap here with gastritis. Again
Speaker 1: h pylori most common cause overall, nothing new that you
Speaker 1: need to know there, Second most common cause, N SAIDs
Speaker 1: an aspirin really easy. You already know this for gastritis,
Speaker 1: So again hpylori most common. N says an aspirin second
Speaker 1: most common. And then another odd bowl that you need
Speaker 1: to know of that's not very common about you know,
Speaker 1: like less than one percent of patients. It's something called
Speaker 1: Zollinger Ellison syndrome and This is a disease that produces
Speaker 1: high levels of gastrin from a neuroendocrine tumor, and gastrin
Speaker 1: leads to high levels of acid in the stomach, which
Speaker 1: can lead to ulcers and gastritis as well as another
Speaker 1: a few other things. So again not a very common cause,
Speaker 1: but something that you do need to know because it
Speaker 1: may come up in the boards, and just a small
Speaker 1: factor that you need to know as well. So hpylori
Speaker 1: is your most common cause overall, but it's going to
Speaker 1: be more associated with duodeno ulcers, where n sets an asper,
Speaker 1: your second most common cause overall is going to be
Speaker 1: more commonly associated with gaster cultures, So just know that,
Speaker 1: but again same overlap with gastritis. Hpylori most common, and
Speaker 1: sayd as an aspirin second most common, and then just
Speaker 1: know about zolinger ellison just as that oddball that may
Speaker 1: come up, as well as some of the other factors
Speaker 1: you know that can lead to pepic ulcers as well.
Speaker 1: Increased alcohol use, smoking also more common and elderly. Those
Speaker 1: are the less less important things that you need to know.
Speaker 1: But of course hpilor and SAIDs know those. Don't forget
Speaker 1: that as far as the history and exam, these patients
Speaker 1: are going to have some again non specific epigastric pain, burning, nausea,
Speaker 1: they may have early satiety.
Speaker 2: Those things aren't that important.
Speaker 1: It's not going to help you differentiate on of it and yet,
Speaker 1: But what you do need to know with this on
Speaker 1: the history and exam is the different presentation. Do oddinal
Speaker 1: ulcers are going to get better with food? Gastric ulcers
Speaker 1: are going to get worse with food. So why does
Speaker 1: that happen? Well, gastric cultures. When you eat, acids obviously
Speaker 1: released to help break down the food, and so the
Speaker 1: ulcers in the stomach you have pain right away. So
Speaker 1: as soon as you eat, immediately these patients start having pain,
Speaker 1: whereas duadinal ulcers obviously a little bit further down the
Speaker 1: GI tract. As you're eating, the food's kind of shut down,
Speaker 1: it's clamped off, it's churning up in there trying to
Speaker 1: break down the food. So all the acids in the stomach,
Speaker 1: but it's not until about two to five hours later
Speaker 1: that the food starts to be released from the stomach
Speaker 1: enters the duodom. Now these patients start to have pain.
Speaker 1: So while these patients are eating and they have a
Speaker 1: duodin ulcer. They have some relief for about two to
Speaker 1: five hours while the acids still sitting in the stomach.
Speaker 2: Once it starts to come out, then they have pain.
Speaker 1: So duodenal ulcers they're gonna have, They're gonna have relief
Speaker 1: with food. They're gonna see their symptoms improved. Duadinals are
Speaker 1: going to be better with food. Gastric is gonna be
Speaker 1: worse with food. The way I remember that duodenal ulcers.
Speaker 1: Du I remember, dude, give me food?
Speaker 2: Do you do?
Speaker 1: Just like in dude and duodenal? Dude give me food?
Speaker 1: So better with food, duodonal ulcers and gastric.
Speaker 2: Is worse with food.
Speaker 1: And that's why patients with gastric ulcers that the pain
Speaker 1: gets worse with eating. A lot of times you'll see
Speaker 1: weight loss in these individuals compared to duaden ulcers. You
Speaker 1: may see weight gain because their symptoms get better with food,
Speaker 1: so they tend to eat more, So it makes sense.
Speaker 2: One other thing to be.
Speaker 1: Mindful of is that peptic ulcers can bleed and they
Speaker 1: can also perforate, So you need to know that peptic
Speaker 1: ulcers are actually peptic ulcer disease is the most common
Speaker 1: cause of an upper GI bleed. Peptic Ulcer disease most
Speaker 1: common cause of an upper GI bleed. And in the
Speaker 1: case that they do perforate, these patients are going to
Speaker 1: go from this kind of vague epigastric pain pepsia blah
Speaker 1: blah blah, to this sudden onset of this sharp, acute
Speaker 1: abdominal pain. They may have signs of peritonitis like rebound
Speaker 1: tenderness guarding. So know that these peptic ulcers can perforate,
Speaker 1: they can bleed, and the presentation is going to be
Speaker 1: much different. It's obviously a much more serious situation as
Speaker 1: far as diagnosing. Ultimately, your most sensitive and specific test
Speaker 1: is going to be in an endoscopy, But there's a
Speaker 1: few things you want to do before you get to
Speaker 1: an endoscopy. But remember, if an endoscopy is on the
Speaker 1: answer listen it says what is your best test endoscopy,
Speaker 1: it's always going to be the endoscopy. But in real life,
Speaker 1: there's a few things that you're going to do first
Speaker 1: and a few other tests. So if it says what's
Speaker 1: your initial test, you may go with some other things.
Speaker 1: So let's go over that Initially you're probably going to
Speaker 1: test for H. Pylori, So you can do that a
Speaker 1: couple of different ways. You can do a urrea breath
Speaker 1: test or an H. Pylori stool antigen H pylori testing.
Speaker 1: When you do a uria breath test, what you need
Speaker 1: to know about this is is that H. Pylori produces
Speaker 1: an enzyme called urease, which breaks down urrea into ammonia
Speaker 1: and carbon dioxide. So the way this test works is
Speaker 1: that during the test, the patient is given a pill
Speaker 1: containing urea and then they blow into this bag. They
Speaker 1: blow into the bag, they close off the bag, it's
Speaker 1: sent to a lab, and then they test for the
Speaker 1: amount of exhaled carbon dioxide. And remember again they were
Speaker 1: given urea, and as I said before, H pylori turns
Speaker 1: urea into carbon dioxide and ammonia. So if there's an
Speaker 1: increase in all this carbon dioxide that's in this bag,
Speaker 1: then obviously this is gonna be a positive test for H.
Speaker 2: Pylori.
Speaker 1: So that's how a urrea breath test works. H Pylori
Speaker 1: stool intogen is straightforward. It's literally just checking for a
Speaker 1: stool antigen of H.
Speaker 2: Pylori.
Speaker 1: So that's another test that you can do as well.
Speaker 1: And then ultimately, like I said before, the gold standard
Speaker 1: test is going to be your endoscopy. That's going to
Speaker 1: be to diagnose. You can visualize the ulcer and you
Speaker 1: can take biopsies if needed, and then treatment depends on
Speaker 1: the cause. So let's start with H pylori. If this
Speaker 1: patient is H pylori positive, again, just like in guesstritis,
Speaker 1: you're going to do quadruple therapy. The way I remember
Speaker 1: quadruple therapy for an hpylori positive patient is I remember
Speaker 1: these patients have belly pain. They want you to treat
Speaker 1: their belly pain so they can get better. So they
Speaker 1: say to you, treat my belly, please, treat my belly please.
Speaker 1: TMBP that stands for tetracycling, metronideisol, bismyth subseliciy, and PPIs
Speaker 1: treat my belly please. Tetracycling, metronide, is al, bismuth, subselicily,
Speaker 1: and P. Those are for your H. Pylori positive patients. Now,
Speaker 1: if these patients are hpylori negative, how do you treat
Speaker 1: their peptic ulcer disease? Well, first, treat the underlying cause.
Speaker 1: If they're taking nsids, they're smokers, they drink a bunch
Speaker 1: of alcohol. You're going to discontinue all those things obviously,
Speaker 1: and then you're going to give them PPIs as well.
Speaker 1: You can also use H two blockers, but realistically, anytime
Speaker 1: you have an option of a PPI or an H
Speaker 1: two blocker, unless there's some contraindication of PPIs, always use PPIs.
Speaker 1: Why is that PPIs are much more effective, and that's because,
Speaker 1: I mean, just really quickly break down the way these
Speaker 1: work and just to give you a little bit about
Speaker 1: the may of the mets. So you have a parietal
Speaker 1: cell in the stomach. The parietal cell has a proton pump.
Speaker 1: That's what shoots out all the hydrochloric acid into the stomach.
Speaker 1: That's where all of your acid in the stomach comes from.
Speaker 1: So how is your prietal cell activated. Well, acetylcholine, histamine,
Speaker 1: and gastrin all activate the prietal cell to pump out
Speaker 1: this acid. An H CH two blocker obviously blocks H
Speaker 1: two and that's histamine, So that's a histamine blocker, So
Speaker 1: it blocks just histamine, but you still have acetocholine and
Speaker 1: gastrine that can activate the parietal cell. So while it
Speaker 1: helps because you stop the histamine from activating the paryal cell.
Speaker 1: Stylcholine and gastrine are still working there to pump out acid,
Speaker 1: so there's still some acid production, Whereas a proton pump
Speaker 1: inhibitor actually completely shuts off the proton pump, so it
Speaker 1: doesn't matter how much is stylcholine, how much histamine, how
Speaker 1: much gastrine is activating that parietal cell. The pump is
Speaker 1: shut off, so no acids coming out. So PPIs are
Speaker 1: much more effective. So remember, if you have an option
Speaker 1: of a PPI or hto blocker, use the PPI. So
Speaker 1: again H pylor negative, treat the underlying cause, give them PPIs.
Speaker 1: That's the treatment. If they're H pylori positive, treat the
Speaker 1: H pylori very easy treatment. And then there's one other
Speaker 1: treatment option that you should probably know. For refractory patients.
Speaker 1: The PPIs aren't working, you discontinued all the ensis, et cetera,
Speaker 1: and they're still having SIN, you can do something called
Speaker 1: the parietal cell veagotomy, which is where they sever the
Speaker 1: vagual nerve, which essentially shuts down the portion of the
Speaker 1: stomach where the parietal cells are located. And this obviously
Speaker 1: leads to decreased acid by about seventy five percent, So
Speaker 1: pretty effective procedure, but it's invasive. Obviously, there's a lot
Speaker 1: of things you want to try before you get to
Speaker 1: a parietal cell vegotamin. This is just going to be
Speaker 1: for your refractory patients. So those are the treatments. Let's
Speaker 1: move on to the home stretch here. The last thing
Speaker 1: we're going to go over, and that's going to be
Speaker 1: pyloric stenosis. So this is going to be a condition
Speaker 1: commonly in newborns. About three to six weeks is going
Speaker 1: to be your most common age range, and it's a
Speaker 1: thickening hypertrophy, a thickening or hypertrophy of the pyloris, which
Speaker 1: is the sphincter, the muscular valve between the stomach and
Speaker 1: the duodenum, so it prevents gastric emptying. Risk factors are
Speaker 1: going to be males four times more common in male,
Speaker 1: so definitely know that males are going to be much
Speaker 1: more common. Look at your vignette. If it's a female,
Speaker 1: you know for a vignette probably and that's so common
Speaker 1: that it's going to be pylar scinosis. Three to six
Speaker 1: weeks is going to be your most common age of presentation.
Speaker 1: Sometimes they'll say three to twelve, but generally three to
Speaker 1: six is the most common. And then first born patients
Speaker 1: are also going to be at a higher risk. And
Speaker 1: then the last thing too, not as you know, not
Speaker 1: as big of a risk as the other ones, but
Speaker 1: macrolide antibiotics, in particular erythromycin within the first two weeks
Speaker 1: of birth can also lead to pyloric stenosis. And this
Speaker 1: is the way it's explained, is most likely due to
Speaker 1: the increased gastric motility with macrolight antibiotics. Erythromycin, even a
Speaker 1: zythromycin can cause this. So the increased gastric motility in
Speaker 1: these drugs can lead to hypertrophy from the pyloris basically
Speaker 1: just being overworked. And it's the same reason that we
Speaker 1: use erythromycin and gastroparesis because it increases the gimotility. So
Speaker 1: if you have a patient under two weeks they give
Speaker 1: them a erythromycin, this may lead to pyloric stenosis. So
Speaker 1: risks again males first born three to six weeks of
Speaker 1: life and macrolide antibiotics in particular erythromycin. All right, So
Speaker 1: as far as the history and the exam. They may
Speaker 1: have some non specific symptoms weight loss, dehydration doesn't matter.
Speaker 1: You don't care about that stuff because it's not going
Speaker 1: to help you differentiate it in Yet, what you need
Speaker 1: to know for pylor ex stenosis, there's two really big
Speaker 1: things you cannot forget. So pilar stenosis non bilious projectile
Speaker 1: vomiting after feeding. That is going to be your vignette
Speaker 1: right there. You can just go ahead and circle pilar stenosis.
Speaker 1: That's gonna be your answer. So you see non bilious
Speaker 1: projectile vomiting after feeding pilar stenosis. So why is it
Speaker 1: non bilious? Well, remember this is an obstruction at the stomach.
Speaker 1: It's at the pylorus, so we're not into the area
Speaker 1: where the bile is coming from the common bioduct. It's
Speaker 1: not evolves. It's an unomal rotation of the small bowel,
Speaker 1: so we're not in the area where the bile is
Speaker 1: being excreted. So it's gonna be non bilious. It's in
Speaker 1: the stomach, So non bilious projectile vomiting after feeding that
Speaker 1: is going to be pathonomoonic, almost as pathonomonic as The
Speaker 1: second thing you need to know for the exam and
Speaker 1: that's going to be an olive shaped mass. So on
Speaker 1: physical exam, we talked about the the pyloris being hypertropheed.
Speaker 1: It's enlarged, and on physical exam, normally you're not gonna
Speaker 1: be able to feel the pylorus. But these patients, because
Speaker 1: it's hypertrop feed, you're actually going to feel this olive
Speaker 1: shaped mass in the epigastric area and it's going to
Speaker 1: feel like a small round mass and it's described as
Speaker 1: an olive shaped mass. If you see this on a vignette,
Speaker 1: you see this or you feel this in real life,
Speaker 1: this is really pathdomonic for the disease. And actually, years ago,
Speaker 1: before ultrasound was around, this would be the only way
Speaker 1: you would diagnose it. If you felt this olive shaped mass,
Speaker 1: they would go right to surgery, you know, after you
Speaker 1: treated them with fluids and things like that. So physical
Speaker 1: exam no non bilious projectile vomiting and no olive shaped mass.
Speaker 1: So those are the two things you need to know
Speaker 1: as far as diagnosing. Ultrasound is going to be your
Speaker 1: test of choice. It's ninety seven to ninety nine percent
Speaker 1: sensitive no radiation.
Speaker 2: These are newborns.
Speaker 1: You really don't want to radiate them if you don't
Speaker 1: have to. And then on the ultrasound, you're going to
Speaker 1: see some pyloric muscle thickness over four millimeters and the
Speaker 1: pyloric canal length will be over seven eighteen millimeters. Don't
Speaker 1: worry about those numbers, but I just want to throw
Speaker 1: that out there so you know that's how you actually
Speaker 1: have a positive ultrasound.
Speaker 2: But ultra sound is gonna be your test of choice.
Speaker 1: The only reason I'm even going to mention an upper
Speaker 1: GI series not so much that you're going to use
Speaker 1: it in real life. It's really only going to be
Speaker 1: if ultrasounds inconclusive, the physical exam is inconclusive. But you
Speaker 1: need to know for the exam because on an upper
Speaker 1: GI series, there's a couple of key terms.
Speaker 2: There's one called a string sign.
Speaker 1: It's not specific only to pyloxynosis, but if you do
Speaker 1: see it in this vignette, this is going to be
Speaker 1: a narrowed area of barium flow. It's literally going to
Speaker 1: look like a string of barium because that hypertro feed
Speaker 1: area only allowing a small amount of barium through. So
Speaker 1: that's a string sign and upper GI. And there's another
Speaker 1: one called a railroad track sign, and this is due
Speaker 1: to the pyloric mucosa compressing and pushing causing this double
Speaker 1: canal where you're going to see two small tracks of
Speaker 1: barium flowing through. It kind of looks like a railroad
Speaker 1: and that's a railroad sign on upper GI. So again
Speaker 1: in real life, probably not going to do an UPPERGI,
Speaker 1: but you do need to know for the exams because
Speaker 1: they like to throw out these key terms of string
Speaker 1: sign and railroad track sign on what you'll see on UPPERGI.
Speaker 1: And then as far as labs, they're vomiting up all
Speaker 1: the stomach acids, so you may have this hypochloromic metabolic acidosis.
Speaker 1: They may also have hypokalmia, and this is just because
Speaker 1: the kidney's compensating and flushing out all of the renal
Speaker 1: potassium excretion. So hypochloromic metabolic acidosis may be seen. And
Speaker 1: then they also may have hypokalemia on labs. But your
Speaker 1: key for diagnosis is going to be your ultrasound. But
Speaker 1: know these things as well. So as far as treatment,
Speaker 1: initially these patients can be kind of sick. They're volume depleted,
Speaker 1: so before you get to any intervention, you need to
Speaker 1: start with some fluids. You want to do electrolyte replacement.
Speaker 1: Remember again I said they may be HYPOKLEMICX you want
Speaker 1: to replace the potassium, may give them some dextros IV
Speaker 1: fluids and things like that. Once they're euvulymic, then you
Speaker 1: get to the actual procedure that needs to be done
Speaker 1: in these patients. And this is called the pyloral miotomy
Speaker 1: is the name of the procedure that you want to
Speaker 1: do once they're stable their euvolemic and this is normally
Speaker 1: done laparoscopically. The surgeon makes this longitudinal incision into the
Speaker 1: pylorus and once they make this longitudinal incision, that hypertrophied
Speaker 1: muscle kind of pops out through this incision that they made.
Speaker 1: And once it pops up through this area of the incision,
Speaker 1: now beneath the area of the incision, there's this canal
Speaker 1: that opened up this new space because all the muscle
Speaker 1: kind of tunneled up through this incision, and they actually
Speaker 1: have this area where the stomach contents can flow through
Speaker 1: this area, so that again it's called a pyloromiotomy. Pyloromotomy
Speaker 1: is going to be the treatment of choice once these
Speaker 1: patients are stable and euvolemic, so that's what you need
Speaker 1: to know. Those are the main things. I feel like
Speaker 1: I kind of touched on all the high yield stuff.
Speaker 1: I hope that was helpful. And as always, good luck
Speaker 1: on your pants, your panry, your ear, and good luck
Speaker 1: in PA school and